AB1626 ASSOCIATION BETWEEN PRIOR SEVERE CUTANEOUS ADVERSE REACTIONS(SCARS) AND SUBSEQUENT AUTOIMMUNE DISEASE RISK: A NATIONWIDE POPULATION-BASED COHORT STUDY
Authors: C. C. Chang, T. M. Lin, C. K. Chang, H. Lee
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Life-threatening severe cutaneous adverse reactions (SCARs) include Stevens-Johnson syndrome/toxic epidermal necrolysis, acute generalized exanthematous pustulosis, and drug-induced hypersensitivity syndrome/drug reaction with eosinophilia and systemic symptoms. Previous report revealed that a gradual loss of regulatory T (Treg) cell function after resolution of SCARs may increase the risk of subsequently developing autoimmune diseases (ADs). The association between patients with SCARs and ADs remain unclear and are scarce. <h3>Objectives</h3> This study explored the association of SCARs with AD risk. <h3>Methods</h3> Individuals with SCARs between 2006 and 2015 were identified and 1:10 matched on age and sex with individuals without SCARs. We performed multivariate and stratified analysis using the Kaplan–Meier method and Cox proportional hazards models in order to estimate the association between SCAR cohort and the risk of developing ADs. <h3>Results</h3> A total of 26844 patients with SCAR and 268440 non-SCAR comparison subjects were selected from NHIRD. For individual organ-specific ADs, SCAR cohort as compared with non-SCAR cohort, adjusted hazard ratio (aHR) were higher for incident autoimmune hemolytic anemia (aHR 3.36, 95% CI: 1.84-6.13), Hashimoto's thyroiditis (aHR 2.26, 95% CI: 1.64-3.12), Henoch-Schonlein purpura (aHR 8.99, 95% CI:6.53-12.4) and inflammatory bowel disease were (aHR 9.78, 95% CI:5.27-18.5) (see Table 1). Furthermore, for individual systemic ADs, SCAR cohort as compared with non-SCAR cohort, aHR were higher for incident ankylosing spondylitis(aHR 1.56), psoriasis(aHR 10.39), polymyositis/dermatomyositis (aHR 10.39), rheumatoid arthritis(aHR 2.48), primary Sjogren syndorme(aHR 5.92), systemic lupus erythematosus(aHR 9.58), systemic sclerosis(aHR 7.56) and systemic vasculitis (aHR 13.54).(see Table 1) <h3>Conclusion</h3> Patients with SCARs have higher risk of ADs than patients with no SCARs. Further mechanistic research should be conducted. <h3>References</h3> [1]Guvenir H, Arikoglu T, Vezir E, Misirlioglu ED. Clinical Phenotypes of Severe Cutaneous Drug Hypersensitivity Reactions. Curr Pharm Des. 2019;25(36):3840-3854. [2]Schopf E, Stuhmer A, Rzany B, Victor N, Zentgraf R, Kapp JF. Toxic epidermal necrolysis and Stevens-Johnson syndrome. An epidemiologic study from West Germany. Arch Dermatol 1991; 127:839–42. [3]Rzany B, Mockenhaupt M, Baur S, Schro¨der W, Stocker U, Mueller J, et al. Epidemiology of erythema exsudativum multiforme majus, Stevens-Johnson syndrome, and toxic epidermal. necrolysis in Germany (1990–1992): Structure and results of a population-based registry. J Clin Epidemiol 1996; 49:769–773. [4]Chan HL, Stern RS, Arndt KA, Arndt KA, Langlois J, Jick SS, et al. The incidence of erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis. A population-based study with particular reference to reactions caused by drugs among outpatients. Arch Dermatol 1990; 126:43–7. [5]Chung WH, Wang CW, Dao RL. Severe cutaneous adverse drug reactions. J Dermatol. (2016) 43:758–66. [6]Wolf R, Orion E, Marcos B, Matz H. Life-threatening acute adverse cutaneous drug reactions. Clin Dermatol 2005;23: 171-81. [7]Sunaga Y, Kurosawa M, Ochiai H, Watanabe H, Sueki H, Azukizawa H, et al. The nationwide epidemiological survey of Stevens-Johnson syndrome and toxic epidermal necrolysis in Japan, 2016-2018. J Dermatol Sci. (2020) 100:175–82. [8]Yang MS, Lee JY, Kim J, Kim GW, Kim BK, Kim JY, et al. Searching for the culprit drugs for Stevens-Johnson syndrome and toxic epidermal necrolysis from a nationwide claim database in Korea. J Allergy Clin Immunol Pract. (2020) 8:690–5. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.